DATE-19/4/2023 MODERATOR- DR JAWAHAR BABU PRESENTOR – KARAN MITTAL Definition • Shock may be defined as the state in which profound and widespread reduction in the effective delivery of oxygen and other nutrients to the tissues leads first to reversible and then, if prolonged, to irreversible cellular injury(HARRISON) • Shock is a state of body in which the supply of blood to the tissues is inadequate to meet the metabolic demands. (ROBBINS) Classification • Hypovolemic Shock • Cardiogenic Shock • Distributive Shock a)Septic Shock b)Anaphylactic Shock c)Neurogenic Shock • Obstructive Shock According to Harrison I. Cardiogenic shock A. myopathic (reduced systolic function) 1. acute myocardial infarction 2. dilated cardiomyopathy 3. myocardial depression in cardiac shock B. Arrhythmic C. Mechanical 1. mitral regurgitation 2. ventricular septal defect 3. ventricular aneurysm II. Extracardiac obstructive shock A. pericardial tamponade B. constructive pericarditis C. pulmonary embolism(massive) D. severe pulmonary hypertension E. coarctation of aorta III. Oligemic shock A. hemorrhage B. fluid depletion IV. Distributive shock A. Septic shock B. Toxic products e.g. overdose C. Anaphylaxis D. Neurogenic shock E. Endocrinologic shock CARDIOGENIC SHOCK • Cardiac output falls due to the pathology in the heart itself and is defined as cardiac index less than 2.2 L/ minute/m2. (Cardiac index is cardiac output per meter of body surface area) • Cardiogenic shock is defined as circulatory failure causing diminished forward flow leading into tissue hypoxia in the setting of adequate intravascular volume with systolic blood pressure < 90 mmHg for 30 minutes;cardiac index < 2.2 L/minute / sq meter; raised PCWP (pulmonary capillary wedge pressure) >15 mmHg. Etiology • Functional Myocardial infarction (most common) Blunt Cardiac Injury (trauma) Myocarditis Cardiomyopathy Septic myocardial depression • Mechanical (Structural) Valvular failure (stenotic or regurgitant) Hypertrophic cardiomyopathy Ventricular septal defect • Arrhythmic Bradycardia Tachycardia CLINICAL FEATURES Cardiovascular Decreased capillary refill May have chest pain Pulmonary Tachypnea Crackles Skin Pallor Renal ↑ sodium and water retention ↓ renal blood flow ↓ urine output Neurologic ↓ cerebral perfusion Anxiety Confusion Agitation Gastrointestinal ↓ bowel sounds Nausea/vomiting Diagnostic findings • ↑ cardiac markers • ↑ BUN • Dysrhythmias • Left ventricular dysfunction on echocardiogram TREATMENT • Correct dysrhythmias • Drug Therapy: Nitrates Inotropes Diuretics Beta blockers • Dobutamine (β1 receptor agonist) is used to raise cardiac output provided there is adequate preload and intravascular volume (it is peripheral vasodilator and reduces BP). • Dopamine is preferred in patients with hypotension. But it may increase peripheral resistance and heart rate worsening cardiac ischemia. Often both dopamine and dobutamine combination may be required. Careful judicial use of epinephrine,norepinephrine, phosphodiesterase inhibitors (amrinone, milrinone) are often needed. Anticoagulants and aspirin are given. Thrombolytics can be used. b blockers,nitrates (nitro-glycerine causes coronary arterial dilatation), ACE inhibitors are also used. • Intra-Aortic Balloon Pump (IABP) May need to be introduced transfemorally as a mechanical circulatory support to raise cardiac output and coronary blood flow • Percutaneous transluminal coronary angioplasty (PTCA) and • Coronary Artery Bypass Graft (CABG) are the final choices. Relief of pain, preserving of remaining myocardium and its function, maintaining adequate preload, oxygenation, minimizing sympathetic stimulation, correction of electrolytes should be the priorities. HYPOVOLEMIC SHOCK A)Haemorrhagic B)Non-Haemorrhagic NON- HAEMORRHAGIC • • External Haemorrhage Vomiting Trauma Diarrhoea Hematoma Polyuria Internal Haemorrhage Dehydration GIT bleeding Burns Hemoperitoneum Third space fluid loss Hemothorax Pathophysiology of hypovolemic shock HYPOVOLEMIA Decreased venous return MULTIORGAN FAILURE Organ dysfunction Perfusion failure and tissue hypoxia Decreased preload DECREASED CARDIAC OUT PUT Hypotension CLINICAL FEATURES • Cardiovascular ↓ preload, stroke volume ↓ capillary refill • Pulmonary Tachypnoea • Renal ↓ urine output • Skin Pallor Cool, clammy • Neurologic Anxiety Confusion Agitation • Gastrointestinal Absent bowel sounds Stage 1 • 15% loss of blood volume – <750 mL – mild hemorrhage • Compensation by peripheral veno-constriction – Normal BP, pulse pressure, respirations – Mild Tachycardia and thirst Stage 2 • 15–30% loss of Circulating blood volume – 750- 1500mL • Tachycardia and tachypnea • Anxiety, confused, slightly pale and cold clammy skin, thirsty • Peripheral veno-constriction may not be sufficient to maintain circulation. • Hence there will be Release of catecholamines • Epinephrine • Norepinephrine and • ADH Stage 3 • 30-40% loss of CBV – 1500-2000 mL • Late decompensation (early irreversible) • Compensatory mechanisms are unable to cope with the loss of blood volume • Weak, thready pulse • Tachypnea • Anxiety, restlessness, aggressive, drowsy • Pale, cool, and clammy skin Stage 4 • >40% CBV loss – >2000 mL • Irreversible – Pulse: Barely palpable – Respiration: Rapid, shallow, and ineffective – Blood pressure becomes low or un-recordable – Lethargic, unresponsive – Renal shut down – Skin: Cool, clammy, and very pale – Multi-organ failure TREATMENT • First objective – reduce or stop further loss of blood • If not possible- lost volume must be replaced fast enough to keep tissues perfused • a. ideally – packed red cells • b. temporary – balanced salt solutions like ringer lactate, normal saline, ringer’s bicarbonate • Kidney functions monitored by indwelling catheter , urinary output 30 -70 ml /hr -if < 30 ml/hr ,increased fluid administration Selection of fluids Fluids must be administered that will concentrate within the body fluid compartment where there is volume deficit. Crystalloids are water-based solutions with small- molecular-weight particles, freely permeable to the capillary membrane. Colloids are water-based solutions with a molecular weight too large to freely pass across the capillary membrane. Crystalloids Ringer lactate Normal saline Dextrose Colloids Dextrans Hydroxyethyl starch (HES) Canine albumin Stroma free haemoglobin Colloids Colloids solutions Crystalloids solutions intravascular volume replacement interstitial volume replacement Initial fluids Isotonic Crystalloid solutions are used for initial resuscitation . The usual initial dose is 1-2 liters for an adult and 20mL/kg for a pediatric patient. Advantages : availability, safety, and low cost. Interstitial losses are replaced. Disadvantages: rapid movement from the intravascular to the extravascular space, leading to three or more times requirement for replacement and resulting in tissue edema. Colloid solutions . More effective in rapidly restoring intravascular volume, requiring less fluid to correct hypovolemia . Includes albumin, hydroxyethyl starch, dextrans, and gelatins. . Limitations: - risk of reaction - expensive 20 Reassessment: Response to initial fluids SEPTIC SHOCK • Sepsis is a life threatening organ dysfunction caused by a dysregulated host response to bacterem or endotoxemia. • It may be produced by gram positive or gram negative bacteria , viruses, fungi or protozoal infections. • Septic shock is defined as the subset of sepsis in which underlying circulatory and cellular or metabolic abnormalities are profound enough to increase mortality substantially. ETIOLOGY Septic shock may be due to gram-positive organisms, gram negative organisms, fungi, viruses or protozoal origin. Gram-negative septicaemia/gram-negative septic shock is called as endotoxic shock. Gram positive septic shock Due to exotoxin by gram +ve bacteraemia like Clostridium tetani/welchii, staphylococci, streptococci pneumococci Fluid loss, hypotension is common; with normal cardiac output Gram negative septic shock Gram negative bacteria cause endotoxemia and its effects. Urinary/gastrointestinal/biliary and respiratory foci are common PATHOPHYSIOLOGY Toxins/endotoxins from organisms like E. Coli, Klebsiella, Pseudomonas, and Proteus Inflammation, cellular activation of macrophages, neutrophils, monocytes Release of cytokines, free radicals Chemotaxis of cells, endothelial injury, altered coagulation cascade—SIRS Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea Severe circulatory failure with MODS (failure of lungs, kidneys, liver, heart) with DIC Hypodynamic, irreversible cold stage of septic shock Septic shock is typically a vasodilatory shock wherein there is peripheral vasodilatation causing hypotension which is resistant to vasopressors. This is due to toxin induced release of isoform of nitric oxide synthetase from the vessel wall which causes sustained prolonged release of high levels of nitric oxide Stages of septic shock a. Hyperdynamic (warm) shock: This stage is reversible stage. Patient is still having inflammatory response and so presents with fever, tachycardia, and tachypnoea. • Pyrogenic response is still intact. Patient should be treated properly at this stage. Based on blood culture, urine culture (depending on the focus of infection), higher antibiotics like third generation cephalosporins, aminoglycosides, metronidazole are started • The underlying cause is treated like draining the pus, laparotomy for peritonitis, etc. Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of sepsis • Hypodynamic hypovolaemic septic shock (cold septic shock): Here pyrogenic response is lost. Patient is in decompensated shock. It is an irreversible stage along with MODS (Multi-organ dysfunction syndrome) with anuria, respiratory failure (cyanosis), jaundice (liver failure), cardiac depression, pulmonary oedema, hypoxia, drowsiness, eventually coma and death occurs (Irreversible stage) Clinical Manifestations of septic shock 1.Early phase: Massive vasodilation – Pink, warm, flushed skin Increased Heart Rate ,Rapid bounding pulse Tachypnea 2.Late phase: Vasoconstriction – Skin is pale & cool Significant tachycardia Decreased BP Decreased Urine output Metabolic & respiratory acidosis with hypoxemia CLINICAL FEATURES • Cardiovascular Biventricular dilation ↓ ejection fraction • Pulmonary Hyperventilation Hypoxemia Respiratory failure ARDS Pulmonary hypertension • Renal Decreased urine output • Skin Warm and flushed; then cool and mottled • Neurologic Alteration in mental status Confusion Agitation coma • Gastrointestinal GI bleeding Diagnostic findings • ↑ WBC • ↓ Platelets • ↑ Lactate • ↑ Glucose • ↑ Urine specific gravity • ↓ Urine sodium • *positive blood cultures* TREATMENT • Correction of fluid and electrolyte by crystalloids, blood transfusion. • Perfusion is very/most important. • Appropriate antibiotics—third generation cephalosporins/ aminoglycosides. • Treat the cause or focus—drainage of an abscess; wound excision • Pus/urine/discharge/bile/blood culture and sensitivity for antibiotics. • Critical care, oxygen, ventilator support, dobutamine/ dopamine/noradrenaline to maintain blood pressure and urine output • Monitoring the patient by pulse oximetry, cardiac status, urine output, arterial blood gas analysis. • Short-term (one or two doses) high dose steroid therapy to control and protect cells from effects of endotoxemia. It improves cardiac, renal and lung functions. • Single dose of methylprednisolone or dexamethasone which often may be repeated again after 4 hours is said to be effective in endotoxic shock. • Activated C protein(Drotrecogin alfa (Xigris)) prevents the release of inflammatory mediators and blocks the effects of these mediators on cellular function NEUROGENIC SHOCK • Sudden loss of vasomotor tone throughout body is known as neurogenic shock • Results from spinal cord trauma (usually T5 or above) or spinal anaesthesia • Injury results in major vasodilation without compensation due to loss of sympathetic nervous system vasoconstrictor tone . • Major vasodilation leads to pooling of blood in the blood vessels, tissue hypoperfusion and ultimately impaired cellular metabolism • It is rarest form of shock • Spinal anesthesia can block transmission of impulses from the SNS resulting in neurogenic shock • When the spinal cord is accidentally injured during surgery ,essentially all cord functions, including the cord reflexes, immediately become depressed to the point of total silence, a reaction called spinal shock CLINICAL FEATURES • Cardiovascular Bradycardia • Pulmonary Dysfunction at level of injury • Renal Bladder dysfunction • Skin ↓ skin perfusion Cool or warm • Neurologic Flaccid paralysis below the level of the lesion/injury Loss of reflex activity • Gastrointestinal Bowel dysfunction Treatment • • • • Airway control should be ensured with spinal immobilization and protection Crystalloid IV fluids should be infused Inotropic agents may be used Severe bradycardia should be treated with Atropine 0.5 to 1.0 mg IV (every 5 min for a total dose of 3.0 mg) • In the presence of Neurologic Deficits, high-dose Methylprednisolone therapy should be instituted within 8 h of injury • A 30 mg/kg bolus should be administered over 15 min followed by a continuous infusion of 5.4 mg/kg per h for the next 2 h ANAPHYLACTIC SHOCK Immediate hypersensitivity reaction (Type I) mediated by the interaction of IgE on mast cells and basophils with the appropriate antigen It primarily results from an antigen-antibody reaction that takes place immediately after an antigen to which the person is sensitive has entered the circulation (Type I hypersensitivity) Primary mediators include Histamine, Serotonin, Eosinophil, Chemotactic Factor, and Proteolytic Enzymes Secondary mediators include PAF, bradykinin, prostaglandins, and leukotrienes. CLINICAL FEATURES • Cardiovascular Chest pain • Pulmonary Swelling to tongue and lips Shortness of breath Edema of larynx and epiglottis Wheezing Rhinitis • Renal Decreased urine output • Skin Flushing Pruritus Urticaria Angioedema • Gastrointestinal Cramping Abdominal pain Nausea Vomiting Diarrhoea • Diagnostic findings Sudden onset History of allergens Exposure to contrast media OBSTRUCTIVE SHOCK A form of cardiogenic shock that results from mechanical impediment to circulation leading to depressed CO rather than primary cardiac failure ETIOLOGY Tension pneumothorax Constrictive pericarditis Cardiac tamponade Intrathoracic obstructive tumours Pulmonary embolus (massive) Acute pulmonary hypertension Aortic dissection TREATMENT General measures ICTD insertion Thoracotomy Pericardiocentesis Embolectomy How to differentiate ? Hypovolemic shock Distributive shock Septic shock History, Hypo-tensive, weak thready pulse, cold and clammy skin, intense thirst, rapid respiration, restlessness, tachycardia, reduced mean arterial pressure Blood volume is normal so no hypotension, skin warm, restlessness, self limiting Presence of nidus of infection(localized or generalized sepsis), warm skin and cardiac output increased initially, later manifestations similar to hypovolemic shock. Cardiogenic shock History, features of hypovolemic shock + congestion of lungs and viscera. REFERENCE • PRINCIPLES OF INTERNAL MEDICINE-HARRISON’S • BASIC PATHOLOGY-ROBBINS • PRINCIPLES AND PRACTICE OF MEDICINE-DAVIDSON’S • PRACTICE OF SURGERY-BAILEY AND LOVE • TEXTBOOK OF MEDICAL PHYSIOLOGY-GUYTON AND HALL
